Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by α₂-adrenergic activation in the lateral parabrachial nucleus

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dc.contributor.authorAndrade, Carina Aparecida Fabricio de [UNESP]
dc.contributor.authorOliveira, Lisandra Brandino de
dc.contributor.authorAndrade-Franzé, Glaucia Maria Fabricio de [UNESP]
dc.contributor.authorLuca Júnior, Laurival Antonio de [UNESP]
dc.contributor.authorColombari, D. S. A. [UNESP]
dc.contributor.authorMenani, J. V. [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de Outo Preto (UFOP)
dc.date.accessioned2015-08-06T16:12:56Z
dc.date.available2015-08-06T16:12:56Z
dc.date.issued2014
dc.description.abstractAlpha2-adrenergic, gabaergic or opioidergic activation in the lateral parabrachial nucleus (LPBN) increases sodium intake. In the present study, we investigated the effects of single or combined blockade of opioidergic and gabaergic receptors in the LPBN on the increase of 0.3 M NaCl intake induced by 2-adrenoceptor activation in the LPBN. Male Holtzman rats (n = 5–9/group) with cannulas implanted bilaterally in the LPBN were treated with the diuretic furosemide (10 mg/kg b wt.) combined with low dose of the angiotensin converting enzyme inhibitor captopril (5 mg/kg b wt.) subcutaneously. Bilateral injections of moxonidine (alpha2-adrenergic/imidazoline receptor agonist, 0.5 nmol) into the LPBN increased furosemide + captopril-induced 0.3 M NaCl intake (25.8 ± 1.4, vs. vehicle: 3.8 ± 1.1 ml/60 min). The opioidergic receptor antagonist naloxone (100 nmol) or the GABAA receptor antagonist bicuculline (5 nmol) injected into the LPBN partially reduced the increase of 0.3 M NaCl intake produced by LPBN moxonidine (11.8 ± 4.0 and 22.8 ± 4.5, respectively, vs. vehicle + moxonidine: 31.6 ± 4.0 ml/60 min, respectively). Similar to the treatment with each antagonist alone, the combined injections of naloxone (100 nmol) and bicuculline (5 nmol) into the LPBN also partially reduced moxonidine effects on 0.3 M NaCl intake (15.5 ± 6.5 ml/60 min). The GABAB receptor antagonist saclofen (5 nmol) injected into the LPBN did not change the effects of moxonidine on 0.3 M NaCl intake (24.3 ± 7.8 ml/120 min). These results suggest that the increase of 0.3 M NaCl intake by 2-adrenergic receptor activation in the LPBN is partially dependent on GABAA and opioid receptor activation in this area.en
dc.description.affiliationUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Fisiologia e Patologia, Araraquara, Rua Humaitá, 1680, Centro, CEP 14801903, SP, Brasil
dc.description.affiliationFederal University of Ouro Preto, Department of Biological Sciences, DECBI-NUPEB, Ouro Preto, MG, Brazil
dc.description.affiliationUnespUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Fisiologia e Patologia, Araraquara, Rua Humaitá, 1680, Centro, CEP 14801903, SP, Brasil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIdFAPESP: 2012/01955-1
dc.description.sponsorshipIdCNPq: 478960/2013-1
dc.format.extent535-541
dc.identifierhttp://www.sciencedirect.com/science/article/pii/S016643281400655X
dc.identifier.citationBehavioural Brain Research, v. 278, p. 535-541, 2014.
dc.identifier.doi10.1016/j.bbr.2014.10.007
dc.identifier.issn0166-4328
dc.identifier.lattes0339253755971890
dc.identifier.lattes1023597870118105
dc.identifier.urihttp://hdl.handle.net/11449/125724
dc.language.isoeng
dc.relation.ispartofBehavioural Brain Research
dc.relation.ispartofjcr3.173
dc.relation.ispartofsjr1,413
dc.rights.accessRightsAcesso restrito
dc.sourceCurrículo Lattes
dc.subjectSodium appetiteen
dc.subjectAdrenergicen
dc.subjectGABAen
dc.subjectOpioiden
dc.subjectDehydrationen
dc.subjectThirsten
dc.titleGabaergic and opioid receptors mediate the facilitation of NaCl intake induced by α₂-adrenergic activation in the lateral parabrachial nucleusen
dc.typeArtigo
unesp.author.lattes0339253755971890
unesp.author.lattes1023597870118105
unesp.author.lattes9055280555067656[1]
unesp.author.orcid0000-0001-8270-265[4]
unesp.author.orcid0000-0003-1167-4441[6]
unesp.author.orcid0000-0003-3393-2202[1]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt
unesp.departmentFisiologia e Patologiapt

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